Cited by 477Nitric Oxide and Endothelin EffectsCellular Mechanics and InteractionsCardiovascular, Neuropeptides, and Oxidative Stress Research

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eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

Balligand, J.-L., Feron, O., Dessy, C.·2009·Physiological Reviews

DOI 10.1152/physrev.00042.2007

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Abstract

Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in…

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Authors: Balligand, J.-L., Feron, O., & Dessy, C.
Affiliations: UCLouvain (BE)
ORCID: Balligand, J.-L.
Dessy, C.
Venue: Physiological Reviews
Publisher: American Physiological Society
Published: 2009-04
Volume: 89
Issue: 2
Pages: 481-534
ISSN: 0031-9333 (ISSN-L)
1522-1210
DOI: 10.1152/physrev.00042.2007
OpenAlex: W2142274635
Cited by: 477
References: 466
Citations by year: 2026: 18 · 2025: 15 · 2024: 14 · 2023: 19 · 2022: 27 · 2021: 22 · 2020: 20 · 2019: 18 · 2018: 30 · 2017: 33 · 2016: 30 · 2015: 34 · 2014: 37 · 2013: 37 · 2012: 38
FWCI: 4.43
Type: journal article
Language: en
Open access: closed
Locations: Physiological Reviews (publishedVersion)
PubMed (publishedVersion)
Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
Keywords: endothelial nitric oxide synthase, mechanotransduction, shear stress, nitric oxide production, endothelial cells, caveolae, signalosome, eNOS phosphorylation, cardiomyocytes, cardiac remodeling, vascular remodeling, progenitor cell mobilization, hypoxia-inducible factor, blood pressure regulation, hemodynamic overload
MeSH terms: Animals, Cardiovascular Physiological Phenomena, Endothelium, Vascular, Humans, Myocardial Contraction, Myocardium, Vasoconstriction, Mechanotransduction, Cellular, Nitric Oxide Synthase Type III

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eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues

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